ABSTRACT
Initial reports suggest an increased thrombotic risk in coronavirus disease 2019 (COVID-19). We present a case of COVID-19 pneumonia that precipitated chest pain, an acute anterior wall ST-elevation myocardial infarction on the fifth day of hospitalization resulting in large left ventricular apical thrombus.
ABSTRACT
In the last decade there have been considerable advances in the understanding of the pathophysiology of malignant ventricular tachyarrhythmias (VA) and Sudden Cardiac Death (SCD). Over 80% of SCD occurs in patients with organic heart disease. However, approximately 10-15% of SCD occurs in the presence of structurally normal heart and the majority of those patients are young. In this group of patients, changes in genes encoding cardiac ion channels produce modification of the function of the channel resulting in an electrophysiological substrate of VA and SCD. Collectively these disorders are referred to as Cardiac Ion Channelopathies. The 4 major syndromes in this group are: The Long QT Syndrome (LQTS), the Brugada Syndrome (BrS), the Short QT Syndrome (SQTS), and the Catecholaminergic Polymorphic VT (CPVT). Each of these syndromes includes multiple subtypes with different and sometimes complex genetic abnormalities of cardiac ion channels. Many are associated with other somatic and neurological abnormalities besides the risk of VA and SCD. The current management of cardiac ion channelopathy could be summarized as follows: 1) in symptomatic patients, the implantable cardioverter defibrillator (ICD) is the only viable option; 2) in asymptomatic patients, risk stratification is necessary followed by the ICD, pharmacotherapy, or a combination of both. A genotype-specific approach to pharmacotherapy requires a thorough understanding of the molecular-cellular basis of arrhythmogenesis in cardiac ion channelopathies as well as the specific drug profile.
Subject(s)
Arrhythmias, Cardiac , Brugada Syndrome/drug therapy , Ion Channels/drug effects , Long QT Syndrome/drug therapy , Adrenergic beta-Antagonists/therapeutic use , Arrhythmias, Cardiac/drug therapy , Arrhythmias, Cardiac/genetics , Arrhythmias, Cardiac/physiopathology , Brugada Syndrome/genetics , Brugada Syndrome/physiopathology , Calcium Channel Blockers/therapeutic use , Humans , Ion Channels/genetics , Ion Channels/physiology , Long QT Syndrome/genetics , Long QT Syndrome/physiopathology , Models, Biological , Potassium Channels/agonists , Sodium Channel Blockers/therapeutic useABSTRACT
INTRODUCTION: Microvolt T wave alternans (TWA) has been proposed as a strong independent predictor of malignant ventricular tachyarrhythmias and sudden cardiac death. TWA reproducibility during bicycle stress test has not been previously investigated. We sought to assess the short-term reproducibility of TWA, as well as heart rate (HR) threshold for TWA, and its spatial distribution and magnitude. METHODS AND RESULTS: The study enrolled 42 patients who were able to complete two bicycle stress tests with HR at peak exercise >110 beats/min within 4 hours of each other and who had technically adequate recordings for TWA analysis during both tests. Concordant results for TWA determination were obtained in 39 (93%) of 42 cases. TWA was present during both tests in 23 patients and was absent during both tests in 16 patients. In the 23 patients with two positive tests, HR at the onset of TWA was not significantly different during the two tests. Further, the number of leads showing TWA and the magnitude of TWA were not significantly different between the two tests. CONCLUSION: TWA is characterized by satisfactory short-term reproducibility and, when present, by high temporal and spatial stability.
Subject(s)
Death, Sudden, Cardiac/prevention & control , Electrocardiography/methods , Tachycardia, Ventricular/diagnosis , Exercise Test , Female , Heart Rate/physiology , Humans , Male , Middle Aged , Reproducibility of Results , Tachycardia, Ventricular/physiopathologyABSTRACT
OBJECTIVE: To report a case of acquired long QT syndrome that, after exclusion of all other possible causes, was probably related to therapy with efavirenz, a novel nonnucleoside reverse transcriptase inhibitor. CASE SUMMARY: This patient presented with recurrent syncope and polymorphic ventricular tachycardia, which was treated with overdrive ventricular pacing and was eliminated by discontinuation of the offending drug. DISCUSSION: This is the first reported case of QT prolongation and severe ventricular arrhythmia associated with the use of efavirenz. The temporal relationship between the initiation of treatment and the onset of electrocardiographic abnormalities, the absence of other apparent precipitating factors, as well as the normalization of QT interval and the resolution of the arrhythmia after discontinuation of the drug, strongly suggest a causal relationship between efavirenz and this adverse clinical event. CONCLUSIONS: Our case shows that any new pharmaceutical compound introduced in clinical practice may potentially result in QT prolongation and life-threatening arrhythmia.
